Although well studied in normal cells, for instance regarding aging and neurodegeneration, diabetes and obesity, it remains unknown what roles PGC1a/TFAM play in tumour progression. Mitochondrial biogenesis has, in addition to PGC1a, in several studies been linked to expression and localisation of oestrogen and oestrogen receptor alpha. The EOC subtypes express ERa at different levels, and expression is lowest in CCC. The aim of this study was to examine the role of mitochondrial regulation in EOC by examining and correlating the expression of the mitochondrial and metabolic Palmatine markers PGC1a, TFAM and ERa in clinical samples, and to relate the expression to EOC subtypes. Furthermore, we examined these markers in an EOC cell line and a multiresistant subline thereof. Formaldehyde is a ubiquitous pollutant in both outdoor and indoor air. It is also an important industrial chemical which has been widely used in Pectolinarin construction, wood processing, carpeting, and so on. As a result, a large number of people are exposed to FA in the environment and/or workplace. FA is known to induce acute poisoning, respiratory irritation, as well as other immunotoxic effects and carcinogesis. It has been classified by the IARC as a human carcinogen that causes nasopharyngeal cancer and potentially leukemia. Risk assessment of FA and leukemia has been challenging due to the inconsistencies in human and animal studies and the unknown mechanisms for leukemia induction. The relationship between FA exposure to respiratory and contact allergies has attracted considerable attention. Accumulating epidemiological evidence suggests that FA is a potential allergen for allergic contact dermatitis. Moreover, it has been shown that the likelihood for the development of allergic asthma increases proportionately with indoor FA concentration. FA could affect the cell counts of different types of immune cells. For instance, it was found that FA could increase the percentage of B cells, but decrease the percentage of total T cells and T-cytotoxic-suppressor cells in the blood of exposed workers, while T-helper-inducer cells remained unchanged.